CSL112 enhances biomarkers of reverse cholesterol transport after single and multiple infusions in healthy subjects

The ability of apolipoprotein A-I (apoA-I) to transport cholesterol from atherosclerotic plaque is thought to underlie its inverse correlation with cardiovascular risk. To gauge the potential of infused apoA-I to transport cholesterol, we quantified cholesterol transport markers in human subjects in...

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Vydané v:	Arteriosclerosis, thrombosis, and vascular biology Ročník 34; číslo 9; s. 2106
Hlavní autori:	Gille, Andreas, Easton, Rachael, D'Andrea, Denise, Wright, Samuel D, Shear, Charles L
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	United States 01.09.2014
Predmet:	Adult Apolipoprotein A-I - metabolism ATP Binding Cassette Transporter 1 - blood Biological Transport Biomarkers Cholesterol - blood Cholesterol Esters - metabolism Cholesterol, HDL - blood Dose-Response Relationship, Drug Female Humans Infusions, Intravenous Lipoproteins, HDL - administration & dosage Lipoproteins, HDL - pharmacokinetics Lipoproteins, HDL - pharmacology Male Phosphatidylcholine-Sterol O-Acyltransferase - metabolism Young Adult reverse cholesterol transport acute coronary syndrome CSL112
ISSN:	1524-4636, 1524-4636
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Abstract	The ability of apolipoprotein A-I (apoA-I) to transport cholesterol from atherosclerotic plaque is thought to underlie its inverse correlation with cardiovascular risk. To gauge the potential of infused apoA-I to transport cholesterol, we quantified cholesterol transport markers in human subjects infused with a novel formulation of apoA-I (CSL112). CSL112 was infused into human subjects in single (57 subjects) and multiple (36 subjects) ascending dose trials. Pharmacokinetic and biomarker assessments were conducted before and after infusions. CSL112 caused an immediate, up to 3-fold elevation of apoA-I and subsequent movement of tissue cholesterol into plasma. Cholesterol appeared first as unesterified cholesterol in the high-density lipoprotein (HDL) fraction and was promptly esterified by lecithin cholesterol acyltransferase. HDL cholesterol increased up to 81±16.5%. Underlying this movement of cholesterol was an immediate and strong rise in the ability of plasma to promote cholesterol efflux from cells ex vivo. CSL112 had its greatest impact on the fraction of efflux mediated by ATP-binding cassette transporter A1 (ABCA1), a cholesterol transporter induced in cholesterol-loaded tissues such as plaque. ABCA1-dependent efflux capacity increased ≤630±421% and total efflux capacity by ≤192±40%. In keeping with this finding, we observed a profound rise in very small HDL, also known as preβ1-HDL, the preferred substrate for ABCA1. Very small HDL increased ≤3596±941%. Elevations in apoA-I, cholesterol efflux, and very small HDL were dose-proportional over a wide range. No significant changes in atherogenic lipids were observed at any dose. Infusion of CSL112 elevates the ability of plasma to withdraw cholesterol from cells. Preferential elevation of ABCA1-dependent efflux may target atherosclerotic plaque for cholesterol removal, making CSL112 a promising candidate therapy for acute coronary syndrome.
AbstractList	The ability of apolipoprotein A-I (apoA-I) to transport cholesterol from atherosclerotic plaque is thought to underlie its inverse correlation with cardiovascular risk. To gauge the potential of infused apoA-I to transport cholesterol, we quantified cholesterol transport markers in human subjects infused with a novel formulation of apoA-I (CSL112).OBJECTIVEThe ability of apolipoprotein A-I (apoA-I) to transport cholesterol from atherosclerotic plaque is thought to underlie its inverse correlation with cardiovascular risk. To gauge the potential of infused apoA-I to transport cholesterol, we quantified cholesterol transport markers in human subjects infused with a novel formulation of apoA-I (CSL112).CSL112 was infused into human subjects in single (57 subjects) and multiple (36 subjects) ascending dose trials. Pharmacokinetic and biomarker assessments were conducted before and after infusions. CSL112 caused an immediate, up to 3-fold elevation of apoA-I and subsequent movement of tissue cholesterol into plasma. Cholesterol appeared first as unesterified cholesterol in the high-density lipoprotein (HDL) fraction and was promptly esterified by lecithin cholesterol acyltransferase. HDL cholesterol increased up to 81±16.5%. Underlying this movement of cholesterol was an immediate and strong rise in the ability of plasma to promote cholesterol efflux from cells ex vivo. CSL112 had its greatest impact on the fraction of efflux mediated by ATP-binding cassette transporter A1 (ABCA1), a cholesterol transporter induced in cholesterol-loaded tissues such as plaque. ABCA1-dependent efflux capacity increased ≤630±421% and total efflux capacity by ≤192±40%. In keeping with this finding, we observed a profound rise in very small HDL, also known as preβ1-HDL, the preferred substrate for ABCA1. Very small HDL increased ≤3596±941%. Elevations in apoA-I, cholesterol efflux, and very small HDL were dose-proportional over a wide range. No significant changes in atherogenic lipids were observed at any dose.APPROACH AND RESULTSCSL112 was infused into human subjects in single (57 subjects) and multiple (36 subjects) ascending dose trials. Pharmacokinetic and biomarker assessments were conducted before and after infusions. CSL112 caused an immediate, up to 3-fold elevation of apoA-I and subsequent movement of tissue cholesterol into plasma. Cholesterol appeared first as unesterified cholesterol in the high-density lipoprotein (HDL) fraction and was promptly esterified by lecithin cholesterol acyltransferase. HDL cholesterol increased up to 81±16.5%. Underlying this movement of cholesterol was an immediate and strong rise in the ability of plasma to promote cholesterol efflux from cells ex vivo. CSL112 had its greatest impact on the fraction of efflux mediated by ATP-binding cassette transporter A1 (ABCA1), a cholesterol transporter induced in cholesterol-loaded tissues such as plaque. ABCA1-dependent efflux capacity increased ≤630±421% and total efflux capacity by ≤192±40%. In keeping with this finding, we observed a profound rise in very small HDL, also known as preβ1-HDL, the preferred substrate for ABCA1. Very small HDL increased ≤3596±941%. Elevations in apoA-I, cholesterol efflux, and very small HDL were dose-proportional over a wide range. No significant changes in atherogenic lipids were observed at any dose.Infusion of CSL112 elevates the ability of plasma to withdraw cholesterol from cells. Preferential elevation of ABCA1-dependent efflux may target atherosclerotic plaque for cholesterol removal, making CSL112 a promising candidate therapy for acute coronary syndrome.CONCLUSIONSInfusion of CSL112 elevates the ability of plasma to withdraw cholesterol from cells. Preferential elevation of ABCA1-dependent efflux may target atherosclerotic plaque for cholesterol removal, making CSL112 a promising candidate therapy for acute coronary syndrome. The ability of apolipoprotein A-I (apoA-I) to transport cholesterol from atherosclerotic plaque is thought to underlie its inverse correlation with cardiovascular risk. To gauge the potential of infused apoA-I to transport cholesterol, we quantified cholesterol transport markers in human subjects infused with a novel formulation of apoA-I (CSL112). CSL112 was infused into human subjects in single (57 subjects) and multiple (36 subjects) ascending dose trials. Pharmacokinetic and biomarker assessments were conducted before and after infusions. CSL112 caused an immediate, up to 3-fold elevation of apoA-I and subsequent movement of tissue cholesterol into plasma. Cholesterol appeared first as unesterified cholesterol in the high-density lipoprotein (HDL) fraction and was promptly esterified by lecithin cholesterol acyltransferase. HDL cholesterol increased up to 81±16.5%. Underlying this movement of cholesterol was an immediate and strong rise in the ability of plasma to promote cholesterol efflux from cells ex vivo. CSL112 had its greatest impact on the fraction of efflux mediated by ATP-binding cassette transporter A1 (ABCA1), a cholesterol transporter induced in cholesterol-loaded tissues such as plaque. ABCA1-dependent efflux capacity increased ≤630±421% and total efflux capacity by ≤192±40%. In keeping with this finding, we observed a profound rise in very small HDL, also known as preβ1-HDL, the preferred substrate for ABCA1. Very small HDL increased ≤3596±941%. Elevations in apoA-I, cholesterol efflux, and very small HDL were dose-proportional over a wide range. No significant changes in atherogenic lipids were observed at any dose. Infusion of CSL112 elevates the ability of plasma to withdraw cholesterol from cells. Preferential elevation of ABCA1-dependent efflux may target atherosclerotic plaque for cholesterol removal, making CSL112 a promising candidate therapy for acute coronary syndrome.
Author	D'Andrea, Denise Gille, Andreas Easton, Rachael Wright, Samuel D Shear, Charles L
Author_xml	– sequence: 1 givenname: Andreas surname: Gille fullname: Gille, Andreas email: andreas.gille@csl.com.au organization: From CSL Limited, Parkville, Victoria, Australia (A.G.); and CSL Behring, King of Prussia, PA (R.E., D.D., S.D.W., C.L.S.). andreas.gille@csl.com.au – sequence: 2 givenname: Rachael surname: Easton fullname: Easton, Rachael organization: From CSL Limited, Parkville, Victoria, Australia (A.G.); and CSL Behring, King of Prussia, PA (R.E., D.D., S.D.W., C.L.S.) – sequence: 3 givenname: Denise surname: D'Andrea fullname: D'Andrea, Denise organization: From CSL Limited, Parkville, Victoria, Australia (A.G.); and CSL Behring, King of Prussia, PA (R.E., D.D., S.D.W., C.L.S.) – sequence: 4 givenname: Samuel D surname: Wright fullname: Wright, Samuel D organization: From CSL Limited, Parkville, Victoria, Australia (A.G.); and CSL Behring, King of Prussia, PA (R.E., D.D., S.D.W., C.L.S.) – sequence: 5 givenname: Charles L surname: Shear fullname: Shear, Charles L organization: From CSL Limited, Parkville, Victoria, Australia (A.G.); and CSL Behring, King of Prussia, PA (R.E., D.D., S.D.W., C.L.S.)
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SubjectTerms	Adult Apolipoprotein A-I - metabolism ATP Binding Cassette Transporter 1 - blood Biological Transport Biomarkers Cholesterol - blood Cholesterol Esters - metabolism Cholesterol, HDL - blood Dose-Response Relationship, Drug Female Humans Infusions, Intravenous Lipoproteins, HDL - administration & dosage Lipoproteins, HDL - pharmacokinetics Lipoproteins, HDL - pharmacology Male Phosphatidylcholine-Sterol O-Acyltransferase - metabolism Young Adult
Title	CSL112 enhances biomarkers of reverse cholesterol transport after single and multiple infusions in healthy subjects
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